In a normal human heart, the sinus node, located generally near the junction of the superior vena cava and the right atrium, acts as the primary natural pacemaker. For a variety of reasons, cardiac rhythm may be compromised if the sinus node malfunctions or its pacemaker activity is supplanted by other activity. For example, a change in autonomic tone can accelerate (e.g., increase in sympathetic activity or decrease in parasympathetic activity) or decelerate (e.g., increase in parasympathetic activity or decrease in sympathetic activity) the sinus node's pacing rate. Further, the presence of an atrial arrhythmia generally indicates that sinus node pacing has been supplanted or become ineffective. In these examples, consequences for one or both atria are apparent; however, profound consequences can also exist for ventricular activity.
In a normal human heart, the atrio-ventricular conduction system provides for coordination between atrial and ventricular activity; however, as discussed above, if the atrial activity is compromised, then a high likelihood exists that ventricular activity will be compromised. In general, the atrio-ventricular conduction system has few inherent mechanisms to prevent inappropriate atrial activity from affecting ventricular activity. The mechanisms that do exist include secondary pacemaker activity and low pass filtering such as 2:1 atrio-ventricular node block, both of which can be affected by or responsive to autonomic activity. To augment or replace these natural mechanisms various artificial mechanisms have been proposed to maintain proper ventricular activity where inappropriate atrial activity exists. Such artificial mechanisms include ablation of the atrio-ventricular node in conjunction with artificial ventricular pacing. Other artificial mechanisms involve direct stimulation of the atrio-ventricular node or parasympathetic nerves to achieve some degree of reversible atrio-ventricular node block. Overall, such mechanisms should consider the complex physiology of the atrio-ventricular node, which can vary considerably from patient to patient.
To overcome various issues associated with artificial control of the atrio-ventricular, mechanisms described herein focus on the His bundle. The His bundle has sparse autonomic innervation and a narrow tubular histology consisting of Purkinje fibers in longitudinal compartments. Various exemplary mechanisms presented herein account for such features and allow for control of conduction through the His bundle.